Objective: To observe the changes of rapidly activated delayed rectifi er potassium channel (IKr)
and slowly activated delayed rectifier potassium channel (IKs) in cardiac hypertrophy and to
evaluate the eff ects of IKr and IKs blocker on the incidence of ventricular arrhythmias in guinea pigs
with left ventricular hypertrophy (LVH). Methods: Guinea pigs were divided into a sham operation group and a left ventricular hypertrophy
(LVH) group. LVH model was prepared. Whole cell patch-clamp technique was used to record IKr
and IKs tail currents in a guinea pig model with LVH. The changes of QTc and the incidence rate of
ventricular arrhythmias in LVH guinea pigs were observed by using the IKr and IKs blockers.
Results: Compared with cardiac cells in the control group, the interventricular septal thickness at
end systole (IVSs), left ventricular posterior wall thickness at end systole (LVPWs), QTc interval
and cell capacitance in guinea pigs with LVH were significantly increased (P<0.05); while IKs
densities were significantly reduced [+60 mV: (0.36±0.03) pA/pF vs (0.58±0.05) pA/pF, P<0.01].
However, LVH exerted no significant effect on IKr densities. IKr blocker markedly prolonged the QTc
interval (P<0.01) and increased the incidence of ventricular arrhythmias in guinea pigs with LVH
compared with the control guinea pigs. In contrast, IKs blocker produced modest increase in QTc
interval in guinea pigs of control group with no increase in LVH animals. IKs blocker did not induce
ventricular arrhythmias incidence in either control or LVH animals.
Conclusion: The cardiac hypertrophy-induced arrhythmogenesis is due to the down-regulation
of IKs.